Journal: Viruses

Article Title: Establishment of a Dual-Reporter Minigenome System for Respiratory Syncytial Virus

doi: 10.3390/v18030304

Figure Lengend Snippet: Mini-NLuc-sfGFP for small-molecule evaluation. ( A ) The experimental protocol involved transfecting the Mini-NLuc-sfGFP minigenome into BSR-T7/5 cells, followed by treatment with a range of small molecules. The inhibitory effects were initially assessed by quantifying the fluorescence intensity or NLuc activity, which led to the selection of promising candidates for further investigation. Created in BioRender. Wu, C. (2026) https://BioRender.com/8qct7m8 . ( B ) AVG-233 reduced the BSR-T7/5 cell viability in a concentration-dependent manner (OD 450 ). ( C ) Similarly, RSV L-protein-IN-4 reduced the BSR-T7/5 cell viability in a concentration-dependent manner (OD 450 ). ( D ) AVG-233 demonstrated a dose-dependent inhibition of Mini-NLuc-sfGFP reporter gene expression, as indicated by the luciferase activity. ( E ) Similarly, RSV L-protein-IN-4 exhibited the dose-dependent inhibition of the Mini-NLuc-sfGFP reporter gene expression, also measured using the luciferase activity. Data are presented as the mean ± SD of three independent experiments, each performed in triplicate.

Article Snippet: Small-molecule inhibitors of RSV L polymerase, namely, AVG-233 (CAS no. 2151937-80-1) and RSV L-protein-IN-4 (CAS no. 851657-60-8), both sourced from Topscience Co. Ltd., China, were diluted in DMSO to create stock solutions at various concentrations.

Techniques: Fluorescence, Activity Assay, Selection, Concentration Assay, Inhibition, Gene Expression, Luciferase

Journal: Viruses

Article Title: Establishment of a Dual-Reporter Minigenome System for Respiratory Syncytial Virus

doi: 10.3390/v18030304

Figure Lengend Snippet: Validation of small-molecule inhibitory effects assessed by Mini-NLuc-sfGFP and confirmed in RSV A2. RSV A2 infection was conducted at a multiplicity of infection (MOI) of 0.1, utilizing a primary antibody of mouse anti-RSV F and a secondary antibody of goat anti-mouse FITC conjugate. ( A ) Immunofluorescence imaging showed that AVG-233 inhibited viral infection at 0, 0.01, 0.05, 0.25, 0.5, 1, 2, and 3 μM. ( B ) Viral genome copy numbers via RT-qPCR at equivalent concentrations. ( C ) Immunofluorescence imaging showed that RSV L-protein-IN-4 inhibited viral infection at 0, 0.01, 0.05, 0.25, 0.5, 1, 2, and 3 μM. ( D ) Viral genome copy numbers via RT-qPCR at equivalent concentrations. Scale bar: 400 μm. Data are presented as the mean ± SD of three independent experiments, each performed in triplicate.

Article Snippet: Small-molecule inhibitors of RSV L polymerase, namely, AVG-233 (CAS no. 2151937-80-1) and RSV L-protein-IN-4 (CAS no. 851657-60-8), both sourced from Topscience Co. Ltd., China, were diluted in DMSO to create stock solutions at various concentrations.

Techniques: Biomarker Discovery, Infection, Immunofluorescence, Imaging, Quantitative RT-PCR

Journal: bioRxiv

Article Title: Acquired resistance to the PRMT5 inhibitor confers collateral sensitivity to MEK inhibition in MTAP-null non-small cell lung cancer

doi: 10.64898/2026.04.16.719008

Figure Lengend Snippet: High-throughput drug screen and MEK inhibitor sensitivity in MRTX1719-resistant NSCLC cells. (A) Composition of the compound library used for drug screen, including SGC epigenetic compounds, FDA-approved oncology drugs, and TargetMol epigenetic inhibitors. (B) IC50 values of MRTX1719 and anisomycin in DMSO and MRTXR cells. Anisomycin was included as a nonselective control in the drug screen. (C) Dose-response curves of DMSO and MRTXR cells treated with the MEK inhibitor selumetinib. Data are presented as mean ± SD. (D) Synergy heatmaps of MRTX1719 and selumetinib in DMSO and MRTXR cells. Synergy mean scores were calculated using the Bliss model with the SynergyFinder+ tool.

Article Snippet: The screening library comprised 619 compounds, including SGC epigenetic compounds, TargetMol epigenetic inhibitors, and FDA-approved oncology drugs ( ).

Techniques: High Throughput Screening Assay, Drug discovery, Control